Genomic evidence of adaptive evolution in the reptilian SOCS gene family

Abstract

The suppressor of the cytokine signaling (SOCS) family of proteins play an essential role in inhibiting cytokine receptor signaling by regulating immune signal pathways. Although SOCS gene functions have been examined extensively, no comprehensive study has been performed on this gene family’s molecular evolution in reptiles. In this study, we identified eight canonical SOCS genes using recently-published reptilian genomes. We used phylogenetic analysis to determine that the SOCS genes had highly conserved evolutionary dynamics that we classified into two types. We identified positive SOCS4 selection signals in whole reptile lineages and SOCS2 selection signals in the crocodilian lineage. Selective pressure analyses using the branch model and Z-test revealed that these genes were under different negative selection pressures compared to reptile lineages. We also concluded that the nature of selection pressure varies across different reptile lineages on SOCS3, and the crocodilian lineage has experienced rapid evolution. Our results may provide a theoretical foundation for further analyses of reptilian SOCS genes’ functional and molecular mechanisms, as well as their roles in reptile growth and development.

Research Advances on Suppressor of Cytokine Signaling 3 (SOCS3) in Animal Carbohydrate and Lipid Metabolism Processes

“…The KIP region is an analogue binding region to JAK kinases of the JAK-STAT signaling pathway. It can competitively inhibit the activity of JAK kinase [2][3][4]19 (Fig. 1 and 2).…”

“…In recent years, researchers have found that the Suppressor of Cytokine Signaling 3 (SOCS3) activated/triggered by leptin signal plays important roles in the cellular energy metabolism, especially in the carbohydrate and lipid metabolism processes [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18] . The SOCS3 is a heterologous multimer in its protein structure, which is composed of a SH2 region, an extended SH2 sub-domain (ESS), a SOCS box and the N-terminal KIP (i.e., kinase identity region) domain (Fig.…”

“…Recently, many studies have found that the inflammatory factors mediate the specific signal transduction of inflammatory response in cells [2][3][4][5][6][7][8][9][10][11][12][13][14][15] , which leads to the phosphorylation of Insulin Receptor Substrate 1 (IRS-l) serine in insulin (INS) sensitive cells (INSSC), such as hepatocytes and adipocytes, through the intracellular inhibitors IL-6 and SOCS3. Subsequently, the signal transduction of inflammatory response inhibits the tyrosine phosphorylation of IRS-l and simultaneously blocks the insulin signal transduction, which induces insulin resistance (IR) [3][4][5][6][7][8][9][10][11][12][13][14][15] . Actually, SOCS3 is a potential inhibitor protein related to obesity, immunity and inflammation.…”

“…3). The SH sites of different SOCS proteins are essential elements for activating the complex of tyrosine phosphorylation receptors and they are key structural motifs for the inhibition of SOCS proteins [2][3][4][5][6] . However, the SH site itself is not enough to inhibit the signal transduction of the JAK-STAT signaling pathway, which requires the involvement of pre-SH sites of the N-terminal regions that are called the kinase inhibition regions 5,6 .…”